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In response to the rising demand for renal transplantations, more marginal organs are being transplanted with the result of decreasing graft survival rates. Ischemia-reperfusion injury (I-R) that occur during the transplantation is considered primarily an inflammatory response to oxidative stress (OxS). The extent of lipid peroxidation (LP) after I-R injury in the kidney has been controversial. Metabolism of oxygen by cells generates potentially deleterious reactive oxygen species, including superoxide anion radical, hydrogen peroxide, and hydroxyl radical. Under normal physiologic conditions the rate and magnitude of oxidant formation is balanced by the rate of oxidant elimination. However, an imbalance between prooxidants and antioxidants results in OxS, which is the pathogenic outcome of the overproduction of oxidants that overwhelms the cellular antioxidant capacity. There is increasing evidence that an elevation of OxS and associated oxidative damages are mediators of vascular injury in various cardiovascular pathologies, including hypertension, atherosclerosis, and ischemia-reperfusion. We have shown recently during our previous work supported by Estonian Science Foundation grant 3959 that angiotensin receptor II antagonist modulated beneficially the oxidative status in the remnant kidney. There is also evidence from other researchers that renin-angiotensin blockade might useful in the prevention of the oxidative damage in remnant and also in reperfused kidney. Therefore, we hypotesized that pretreatment with angiotensin II receptor blocking agent alone or in the combination with statin and antioxidant might be effective to potentiate antioxidative resources of the I-R damaged kidney compared with controls. We further would aim to investigate the relationship between the inflammation, renin-angiotensin system and oxidative stress by determing renin-angiotensin components, LP and antioxidant defence markers in rats with and without treatments. |